Toward an Integrative Model of Flashbacks — The Hippocampal Drive for Coherence

Objective To propose a revised neurobiological framework for traumatic memory that explains the phenomenology of flashbacks not as mere reactivations of fear circuits, but as the hippocampal complex’s ongoing attempt to integrate unprocessed sensory–emotional fragments encoded without temporal context during extreme stress. Background Classical models—the fear-network theory (Foa & Kozak, 1986) and the dual-representation theory (Brewin et al., 1996, 2010)—conceptualize flashbacks as intrusive replays of amygdala-driven sensory representations that fail to link with hippocampal–prefrontal systems. These frameworks accurately describe fragmentation but overlook the hippocampus’s potential active role in later integration. Neurobiological and computational findings across the last two decades show that traumatic stress disrupts prefrontal inhibition, amygdala dominance, and hippocampal contextual encoding, resulting in memories stripped of temporal and narrative structure. The persistence of flashbacks despite safety suggests a dynamic process rather than a static lesion. Methods / Theoretical Approach This chapter synthesizes evidence from functional neuroimaging, neuroendocrinology, and predictive-coding theory to construct a tri-systemic model of trauma involving the medial prefrontal cortex, amygdala, and hippocampus. The analysis follows the chronological breakdown of this system under threat—prefrontal disinhibition, amygdala hyper-encoding, HPA-axis discontrol, and hippocampal silencing—and explores subsequent re-engagement mechanisms. Results / Proposed Mechanism Flashbacks are conceptualized as failed integration events: partial hippocampal reactivation of unbound sensory–emotional traces in the absence of temporal coding. This re-engagement triggers amygdala-mediated affective flooding, creating the illusion of present-tense re-living. Conclusions / Implications Re-experiencing may represent a neural system striving for coherence, not solely pathology. Understanding flashbacks as integration attempts clarifies why they can emerge during calm, why therapies restoring safety and context diminish them, and how hippocampal–prefrontal synchronization transforms traumatic immediacy into autobiographical memory. This model reframes trauma as a process of disrupted, yet potentially recoverable, neurobiological integration.